This kit is designed to detect antibodies directed against Maedi-visna virus (MVV) or caprine arthritis encephalitis virus (CAEV) in sheep and goat serum, plasma or milk samples. It is based on an indirect ELISA technique, using a mix of MVV/CAEV synthetic peptides.
Contents of Kit
1. MVV/CAEV synthetic peptides coated microplates (screening) 2. Concentrated Conjugate (10×) 3. Positive Control 4. Negative Control 5. Dilution Buffer 14 6. Dilution Buffer 3 7. Wash Concentrate (20×) 8. Substrate Solution (TMB) 9. Stop Solution (0.5 M) * Quantities supplied are indicated on the kit label.
Storage
1. The conjugate, the controls and the substrate solution must be stored at 5°C (± 3°C). 2. Other reagents can be stored between +2°C and +26°C.
General Notes
Infectious Disease ELISA Kits
Citations
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Background
Maedi-visna virus (MVV) and caprine arthritis encephalitis virus (CAEV) are lentiviruses that infect goats and sheep, causing persistent and progressive infections affecting multiple body systems. These viruses are closely related and can cross the species barrier, collectively known as small-ruminant lentiviruses (SRLV). They primarily target monocytes and macrophages in the body and have a specific affinity for certain organs, although the mechanisms behind this targeting are not fully understood. SRLVs are classified into five genotypes (A, B, C, D, and E) based on their phylogenetic relationships. Genotype A includes MVV strains, genotype B includes CAEV strains, genotype C corresponds to SRLV strains found in Norwegian sheep and goats, genotype D is associated with SRLV strains from Spanish and Swiss sheep, and genotype E has been identified in Italy. This classification helps in understanding the genetic diversity and evolutionary relationships among different SRLV strains.
The clinical manifestations of SRLV infection include interstitial pneumonia, meningoencephalitis (inflammation of the brain and meninges), indurative mastitis (chronic inflammation of the mammary gland), and non-suppurative arthritis (inflammation of the joints without the presence of pus). SRLV typically result in latent infections, where most infected animals show no outward symptoms. However, both asymptomatic and symptomatic individuals carry the virus for their entire lives. The virus can be found in their secretions, milk, and colostrum, which serves as a source of infection for their offspring and other animals within the flock or herd.
Figure 1. Cross-species transmission of SRLVs in domestic and wild ruminants. (Source: Minardi da Cruz, J. C. et al., 2013)
Controlling the spread of SRLV is challenging due to the persistent nature of the infection and the lack of available vaccines or specific treatments. Eradication programs rely on the identification and removal of viral carriers from the flock. This involves serological testing to detect the presence of SRLV-specific antibodies in infected animals, as most infected sheep or goats develop a humoral immune response against the virus. Serological techniques, such as enzyme-linked immunosorbent assay (ELISA), are commonly used to detect anti-virus antibodies, providing valuable information for the diagnosis and surveillance of SRLV infection.
1. Minardi da Cruz J C, et al. Small ruminant lentiviruses (SRLVs) break the species barrier to acquire new host range. Viruses. 2013, 5(7): 1867-1884.
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References
Small ruminant lentivirus–induced arthritis: clinicopathologic findings in sheep infected by a highly replicative SRLV B2 genotype
Veterinary Pathology
Authors: Pérez, M., Biescas, E., Reina, R., Glaria, I., Marín, B., Marquina, A., Luján, L.
We describe the clinicopathologic features of an arthritis outbreak in sheep induced by small ruminant lentivirus (SRLV), linked to the presence of a new SRLV isolate phylogenetically assigned to caprine arthritis encephalitis virus–like subgroup B2. Thirteen SRLV seropositive Rasa Aragonesa adult ewes were selected from 5 SRLV highly infected flocks (mean seroprevalence, 90.7%) for presenting uni- or bilateral chronic arthritis in the carpal joint. A complete study was performed, including symptomatology, histopathology, immunocytochemistry, immunohistochemistry, in situ hybridization, and microbiology. The carpus was the joint almost exclusively affected, with 10 sheep (76%) showing a moderate increase in carpal joint size (diameter range, 18–20 cm; normal range, 15–16 cm) without signs of locomotion problems and with 3 ewes (23%) showing severe inflammation with marked increase in diameter (21–24 cm), pain at palpation, and abnormal standing position. Grossly, chronic proliferative arthritis was observed in affected joints characterized by an increased thickness of the synovial capsule and synovial membrane proliferation. Microscopically, synovial membrane inflammation and proliferation and hyperplasia of synoviocytes were observed. More positive cases of SLRV infection were detected by immunocytochemistry of articular fluid than of bronchoalveolar lavage fluid. Immunohistochemistry and in situ hybridization also detected positive cells in the subsynovial connective tissue, lung, mediastinal lymph node, mammary gland, and mammary lymph node. All animals were negative for the presence of Mycoplasma or other bacteria in the articular space. The present outbreak likely represents an adaptation of a caprine virus to sheep. Our results underline the importance of the arthritis induced by SRLV in sheep, a clinical form that might be underestimated.
Maedi-Visna virus (MVV) and caprine arthritis-encephalitis virus are commonly known as small ruminant lentiviruses (SRLVs) due to their genetic, structural, and pathogenic similarities. They produce lifelong lasting infections in their hosts, which are characterized by slow progression till overt disease happens. There are four major clinical forms derived from a chronic inflammatory response due to the constant low grade production of viruses from monocyte-derived macrophages: respiratory (caused by interstitial pneumonia), mammary (which may produce a decrease in milk production due to subclinical mastitis), joint (characterized by lameness), and neurological (characterized by chronic nonpurulent meningoencephalomyelitis). There are three levels which try to eliminate the virus: cellular, body, and the flock level. However, SRLVs have ways to counteract these defenses. This review examines some of them.
COA
Publication 
Figure 1. Cross-species transmission of SRLVs in domestic and wild ruminants.
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